Recent studies suggest that a Th2-skewed chemokine signature in the TME (including elevated CCR4 ligands such as CCL17/CCL22) may correlate with reduced benefit from immune checkpoint blockade in CTCL, consistent with the concept that chemokine-driven immune exclusion and regulatory programs can dampen effective anti-tumor immunity. The gene discussed is CCL22; the disease is primary cutaneous T-cell non-Hodgkin lymphoma.